The present invention relates to a method of modulating the level of lipid metabolites associated with gastrointestinal inflammation to improve animal body weight uniformity in a group of animals and to increase animal carcass yield.
Body weight uniformity is important to meat-type animals going to slaughter. A high level of body weight uniformity facilitates automation of the slaughtering process and reduces meat processing cost at both the pre-slaughter sorting stage and the slaughter stage. Also, animals raised together often compete with each other for space, feed and water. A more uniform body weight among the animals reduces competition and tends to standardize growth within the group.
Body weight uniformity is also important to groups of animals raised for egg production (e.g., laying hens and duck, turkey and chicken breeders). Peak feed allowance is often provided to a whole group of animals at an estimated egg production stage (e.g., when the whole group reaches 45% egg production). Since egg production age correlates well with body weight, a less uniform body weight for the group means that when peak allowance is provided, the heavy, early maturing animals are close to peak egg production while the smaller immature animals are not yet laying. As a result, the heavy, early maturing animals are underfed and the smaller immature animals are overfed. Improving body weight uniformity will minimize the problem.
Enhancing animal carcass yield is also important to the animal meat industry. Using the poultry industry in the United States as an example, approximately eight billion broilers are raised annually. Therefore, even a slight increase in carcass yield can have a significant economic impact.
Reducing bioavailability of a prostaglandin or leukotriene precursor and thus gastrointestinal inflammation in an animal enhances animal growth and improves feed efficiency. See U.S. Pat. Nos. 6,213,930 and 6,383,485, both incorporated herein by reference in their entirety. However, it is not known or readily predictable whether reducing bioavailability of a prostaglandin or leukotriene precursor can improve animal body weight uniformity or increase animal carcass yield.
Prostaglandins and leukotrienes are lipid metabolites involved in gastrointestinal inflammation. Lipid metabolites isoprostanes may also be involved in gastrointestinal inflammation. Prostaglandins, leukotrienes and isoprostanes can be generated from arachidonic acid in animals. Arachidonic acid is released (as arachidonate) from the sn-2 position of membrane phospholipids by phospholipase A2 (PLA2) and then converted into precursors of biologically active prostaglandins and leukotrienes by lipoxygenase or cyclooxygenase. Since animal feed typically contains a high level of linoleic acid which can be easily converted to arachidonic acid, animals fed with such feed have high levels of prostaglandin and leukotriene precursors ready to be converted to prostaglandins and leukotrienes. Arachidonic acid (released as arachidonate) can also be autooxidized nonenzymatically or oxidized enzymatically into isoprostanes, especially when the activity of lipoxygenase and cyclooxygenase are blocked.
Prostaglandins cause inflammatory effects during gastrointestinal traumas, such as colitis and ulcers, and are involved in vasodilation, vasoconstriction, and stimulation of intestinal or bronchial smooth muscle. Prostaglandins are found in inflammatory exudates and can induce fever and erythema. Leukotrienes cause contraction of smooth muscle, such as intestinal smooth muscle, attract leukocytes and increase vascular permeability. Isoprostanes have vasoconstrictive action on select tissues.